早期帕金森病患者快速眼动睡眠期行为障碍研究

目的探讨早期帕金森病患者快速眼动睡眠期行为障碍发生情况,以及帕金森病运动症状、非运动症状和快速眼动睡眠期行为障碍特点。方法共60例原发性帕金森病患者,采用统一帕金森病评价量表第二和第三部分(UPDRSⅡ和UPDRSⅢ)以及Hoehn-Yahr分期评价帕金森病非运动症状和运动症状,蒙特利尔认知评价量表评价认知功能,汉密尔顿焦虑量表和汉密尔顿抑郁量表评价焦虑和抑郁症状;中文版快速眼动睡眠期行为障碍筛查量表判断是否伴快速眼动睡眠期行为障碍,Epworth嗜睡量表(ESS)评价白天过度嗜睡程度;多导睡眠图监测睡眠障碍特征,包括下颌位相性肌电活动密度和快速眼动睡眠期肌肉失弛缓。结果 60例帕金森病患者中42例(70%)伴快速眼动睡眠期行为障碍(PD+RBD组),多导睡眠图监测其异常行为主要表现为上肢伸展抓握、肢体震颤抽搐、发笑、喊叫和怒骂等非暴力动作,仅2例出现暴力击打、蹬踢等异常行为。PD+RBD组患者年龄(P=0.024)、病程8年比例(P=0.000)、UPDRSⅡ(P=0.005)和UPDRSⅢ(P=0.001)评分、Hoehn-Yahr分期2级比例(P=0.007)、焦虑障碍(P=0.044)和抑郁障碍(P=0.001)比例,以及下颌位相性肌电活动密度(P=0.000)和快速眼动睡眠期肌肉失弛缓比例(P=0.000)均高于对照组,其中,PD+RBD组有16例(38.10%)快速眼动睡眠期行为障碍症状早于帕金森样症状5.20(3.91,6.51)年。结论年龄大、病程长、运动症状和非运动症状严重的帕金森病患者易伴发快速眼动睡眠期行为障碍,快速眼动睡眠期行为障碍可能是帕金森病的早期表现。多导睡眠图监测对早期帕金森病伴快速眼动睡眠期行为障碍的诊断有重要参考价值。     

帕金森病两种常见睡眠障碍关联性研究

研究背景阻塞性睡眠呼吸暂停低通气综合征(OSAHS)和快速眼动睡眠期行为障碍(RBD)是帕金森病(PD)两种常见睡眠障碍,本研究探讨帕金森病合并两种睡眠障碍的临床特点和睡眠参数变化,以及二者之间相互作用机制。方法采用统一帕金森病评价量表(UPDRS)、简易智能状态检查量表(MMSE)和蒙特利尔认知评价量表(MoCA)中文版、Epworth嗜睡量表(ESS)和匹兹堡睡眠质量指数(PSQI)、非运动症状问卷(NMSQuest)、帕金森病预后量表-自主神经功能部分(SCOPA-AUT)、39项帕金森病调查表(PDQ-39)和Hoehn-Yahr分期评价190例帕金森病患者运动症状、非运动症状(认知功能、睡眠质量、自主神经功能等)和病情严重程度,并行多导睡眠图监测记录睡眠参数。结果共73例合并阻塞性睡眠呼吸暂停低通气综合征患者,其中22例同时发生快速眼动睡眠期行为障碍(PD+OSAHS+RBD组),51例不发生快速眼动睡眠期行为障碍(PD+OSAHS-RBD组)。PD+OSAHS+RBD组患者UPDRSⅠ评分(P=0.015)、UPDRSⅡ评分(P=0.023)、ESS评分(P=0.002)、PSQI评分(P=0.048)、NMSQuest评分(P=0.001)和SCOPA-AUT评分(P=0.026),以及平均动脉血氧饱和度(P=0.029)、最低动脉血氧饱和度(P=0.001)、快速眼动睡眠期最低动脉血氧饱和度(P=0.000)、快速眼动睡眠期紧张性(P=0.000)和时相性(P=0.000)下颏肌电活动均高于PD+OSAHS-RBD组,而MoCA评分低于PD+OSAHS-RBD组(P=0.013)。相关分析显示,呼吸暂停低通气指数和氧减指数与NMSQuest(r_s=0.252,P=0.032;r_s=0.229,P=0.010)、SCOPA-AUT(r_s=0.322,P=0.005;r_s=0.247,P=0.037)和PDQ-39(r_s=0.340,P=0.004;r_s=0.269,P=0.023)评分呈正相关关系。结论帕金森病同时合并阻塞性睡眠呼吸暂停低通气综合征和快速眼动睡眠期行为障碍的患者认知功能障碍、日间嗜睡程度、自主神经功能障碍等非运动症状更加严重。尽管发生快速眼动睡眠期行为障碍的患者夜间动脉血氧饱和度较高,但并不能显著改善帕金森病合并阻塞性睡眠呼吸暂停低通气综合征患者总体缺氧症状。     

伴睡眠周期性肢体运动的帕金森病患者睡眠结构分析

目的探讨帕金森病(PD)患者中周期性肢体运动(PLM)对夜间睡眠结构的影响。方法收集2018年1月至2020年12月在我院进行多导睡眠监测(PSG)的27例PD患者。患者再以睡眠周期性肢体运动事件指数(PLMSI) 15次/h为界分成两组:PLMSI+组(PLMSI≥15次/h)、PLMSI-组(PLMSI 15次/h)。比较两组之间的睡眠结构。结果两组比较,PLMI+组的觉醒指数升高,非快速眼动Ⅲ期(NREM-Ⅲ)睡眠比例减少,差异有统计学意义(P 0.05);其他睡眠期及睡眠效率的差异无统计学意义(P值均 0.05)。PLMSI+组合并快速眼动期睡眠行为异常(RBD)比率显著高于PLMSI-组(P 0.05)。结论研究表明频繁睡眠周期性肢体运动的帕金森病患者,客观存在睡眠结构紊乱更严重,RBD患病率更高。     

阻塞性睡眠呼吸暂停及快动眼睡眠期行为障碍对帕金森病患者认知功能的影响

目的观察伴阻塞性睡眠呼吸暂停(OSA)及快动眼睡眠期行为障碍(RBD)对帕金森病(PD)患者认知功能的影响。方法收集101例PD患者的临床资料,采用MMSE、蒙特利尔认知评估量表(MoCA)北京版评定患者认知功能,并对患者进行整夜多导睡眠监测(PSG)并对相关结果进行比较。结果根据PSG监测结果,将患者分为对照组34例、OSA组18例、RBD组34例及OSA+RBD组15例。与对照组比较,RBD组及OSA+RBD组MoCA评分显著降低(均P0.05)。与OSA+RBD组比较,RBD组体质量指数及PD组Epworth嗜睡量表评分显著降低,RBD组慢波睡眠比例显著升高(均P0.05)。与OSA组及OSA+RBD组比较,对照组及RBD组呼吸暂停低通气指数及氧减指数显著降低,最低脉搏氧饱和度显著升高(均P0.05);OSA组的觉醒次数较其他三组显著升高(均P0.05)。在相关分析中,PD患者的MoCA评分与RBD(r=0.324,P=0.001)、总睡眠时间(r=0.212,P=0.035)、睡眠效率(r=0.272,P=0.006)、非快速眼动睡眠2期时间(r=0.257,P=0.010)呈正相关。结论认知功能障碍在伴RBD的PD患者中很常见。PD患者认知功能与睡眠效率、总睡眠时间、非快速眼动睡眠2期时间及RBD显著相关。     

帕金森病合并快速眼球运动睡眠行为障碍患者的客观睡眠结构及认知功能

目的 评价帕金森病合并快速眼球运动睡眠行为障碍(RBD)患者的睡眠结构及认知功能,并探讨其睡眠结构与认知功能之间的相关性.方法 本研究为横断面研究,以在我院睡眠中心进行睡眠监测的39例帕金森病合并RBD患者作为病例组,并以年龄、性别相匹配的21例原发性快速眼球运动睡眠行为障碍(iRBD)患者及37例不合并RBD的帕金森病患者作为对照组.所有患者均行整夜睡眠监测以定量睡眠相关参数,并且于监测当天使用蒙特利尔(MoCA)评估量表评估其认知功能.采用多重线性回归分析量表得分与睡眠结构之间的相关性.结果 (1)帕金森病合并RBD患者的睡眠效率(60.9％±16.9％)、总睡眠时间[(329.7±96.5)min]、非快速眼动睡眠2期时间[(127.6±67.6) min]及快速眼动睡眠期时间[(45.3 ±33.2) min]较iRBD组的相应值[77.8％±16.9％以及(397.1 ±88.9)、(188.0±94.7)、(70.6 ±25.9) min]比较明显减少(均P＜0.05),较不合并RBD的PD组的相应值[61.3％±21.7％以及(324.9 ±134.6)、(132.6 ±65.6)、(47.1±31.9)min]减少,但差异均无统计学意义.3组的睡眠潜伏期、快速眼球运动睡眠潜伏期、非快速眼球运动睡眠1期,慢波睡眠比例、氧减指数、呼吸暂停低通气指数及周期性肢体运动指数比较差异均无统计学意义.(2)帕金森病合并RBD患者认知功能最差,其中视空间与执行功能得分[(3.8±1.1)分]较iRBD组[(4.4±0.7)分]比较差异有统计学意义(F=3.426,P＜0.05).(3)多重线性回归显示帕金森病合并RBD患者的RBD病程、睡眠效率和非快速眼动睡眠2期与视空间与执行功能得分有相关性.结论 帕金森病合并RBD患者的睡眠效率、总睡眠、非快速眼动睡眠2期及快速眼动睡眠期时间和认知功能均明显下降,认知功能的改变与睡眠结构的变化可能存在相关性.     

帕金森病睡眠障碍主观与客观评价研究

研究背景 睡眠障碍是帕金森病患者常见的非运动症状之一,其评价方法包括主观量表和客观检查。目前我国对帕金森病睡眠障碍的研究主要以单一主观量表观察或多导睡眠图监测的客观方法为主,不能全面反映患者病情。本研究采用匹兹堡睡眠质量指数(PSQI)与多导睡眠图监测相结合的方法评价帕金森病患者睡眠情况,以分析其临床特点,探讨主观量表评价方法与客观检查方法之间的差异性及一致性。方法 选择116例帕金森病患者,进行PSQI评分及多导睡眠图监测,于病情"开"期进行统一帕金森病评价量表(UPDRS)评分及HoehnYahr分级,以及抑郁症状[汉密尔顿抑郁量表(HAMD,24项)]、认知功能[蒙特利尔认知评价量表(MoCA,北京版)]和嗜睡症状[Epworth嗜睡量表(ESS)]评价。结果 根据PSQI评分,选择有睡眠障碍(PSQI≥7分)和无睡眠障碍(PSQI<7分)患者各58例(50%)。与无睡眠障碍组相比,睡眠障碍组患者MoCA评分降低(23.34±3.50对24.89±3.52;t=2.377,P=0.019),UPDRSⅠ[4.00(2.00,5.00)对3.00(2.00,5.00);U=2.306,P=0.021]和Ⅱ评分[12.00(9.00,16.00)对10.00(6.00,13.00);U=1.995,P=0.046]增加,左旋多巴日等效剂量增加[(508.14±335.85)对(394.06±236.42)mg/d;t=2.115,P=0.037)];虽然UPDRSⅢ评分及HoehnYahr分级亦有所增加,但差异无统计学意义(P>0.05)。多导睡眠图监测显示,睡眠障碍组患者总睡眠时间减少、睡眠效率降低、睡眠潜伏期延长、非快速眼动睡眠期Ⅱ期时间减少(均P<0.05);但两组患者快速眼动睡眠潜伏期、觉醒次数、非快速眼动睡眠期Ⅰ期时间和比例、慢波睡眠比例、快速眼动睡眠期时间和比例、睡眠中周期性肢体运动指数、快速眼动睡眠期行为障碍发生率、氧减指数、最低血氧饱和度及睡眠呼吸暂停低通气指数差异均无统计学意义(P>0.05)。PSQI评分分别与ESS(r=0.200,P=0.032)、HAMD(r=0.202,P=0.030)、UPDRSⅠ(rs=0.266,P=0.004)和Ⅱ评分(rs=0.254,P=0.007)、左旋多巴日等效剂量(r=0.213,P=0.022)及睡眠潜伏期(rs=0.211,P=0.023)等因素呈正相关;而与总睡眠时间(r=0.231,P=0.003)、睡眠效率(r=0.192,P=0.039)、MoCA评分(r=0.236,P=0.011)呈负相关。结论 当帕金森病患者出现睡眠障碍时,其认知损害加剧、思维和情绪障碍常见、左旋多巴日等效剂量增大,多项客观睡眠参数呈病理性改变,且睡眠障碍程度与这些因素均有关联性。无论是主观或客观评价方法评价帕金森病患者总体睡眠质量均具有较好的一致性,但了解睡眠结构紊乱程度及筛查其他睡眠障碍性疾病仍需进行多导睡眠图监测。     

帕金森病患者睡眠障碍的多导睡眠图、多次睡眠潜伏期试验分析

目的 使用多导睡眠图、多次睡眠潜伏期试验客观分析帕金森病(PD)患者睡眠障碍特征.方法 对26例临床确诊的PD患者(PD组)和31名无明显中枢神经系统疾病的对照者(对照组)行全夜可移动视频多导睡眠监测及次日多次睡眠潜伏期试验,分析比较2组患者睡眠结构及平均睡眠潜伏期、入睡期快速眼球运动(REM)睡眠(SOREMPs)、睡眠发作(Sas)情况.结果 PD组N2睡眠期百分比(32.8%±13.1%)、REM睡眠期百分比(8.6%±5.3%)、平均睡眠潜伏期[(9.6±4.4)min]较对照组[40.2%±9.1%、11.5%±5.1%、(15.7±3.1)min]明显降低(t=-2.515、-2.054、-6.164,P＜0.05),PD组醒觉指数[(41.8±32.1)次/h]较对照组[(28.6±11.0)次/h]明显升高(t=2.151,P＜0.05).PD患者中出现日间过度瞌睡(EDS)7例(7/26,26.9%),明显高于对照组(1/31,3.2%;×2=4.764,P＜0.05).多元逐步线性回归分析显示校正睡眠效率、呼吸暂停低通气指数、醒觉指数,PD患者平均睡眠潜伏期的缩短与年龄(β=-0.328)、左旋多巴等效剂量(β=-0.008)的增加呈线性相关(t=-2.829、-2.352,均P＜0.05).PD组有5例(5/26,19.2%)出现SOREMPs,3例(11.5%)出现Sas,而对照组均无出现SOREMPs和Sas.结论 PD患者睡眠结构改变和EDS较常见,虽然PD患者中Sas不多见,但临床医师需提高警惕.     

快速眼动睡眠期行为障碍与神经变性病发病机制研究进展

快速眼动睡眠期行为障碍系指快速眼动睡眠期肌肉失弛缓,并出现梦境(通常是暴力梦境)相关肢体运动(梦境演绎行为)。其人群发病率为0.38%~2.01%,在神经变性病尤其是α-突触核蛋白病患者中的发病率明显增加。快速眼动睡眠期行为障碍可早于α-突触核蛋白病数十年出现,因此可以作为预测神经变性病的早期标记。本文拟就近年来关于快速眼动睡眠期行为障碍发病机制及其与神经变性病之间的关系进行简要综述。     

帕金森病患者快速眼动期睡眠行为障碍的多项睡眠图分析

目的:客观地分析帕金森病(PD)患者快速眼动期睡眠行为障碍(RBD)的多项睡眠图(PSG)表现.方法:采用UPDRS -Ⅲ评分、Hoehn -Yahr评分及用药调查表分别对28例PD患者的疾病严重程度、病程、多巴胺能药物应用等情况进行评定和计算,并结合全夜可移动的同步视频多项睡眠图(V-PSG)监测进行分析比较各项睡眠结构、睡眠进程以及睡眠相关事件.结果:利用同步V-PSG并结合临床病史,发现28例PD患者中有14例(占50%)伴有RBD.PD伴RBD组的病程[(6.76±3.44)年]较PD不伴RBD组病程[(2.96±1.99)年]长,其Hoehn -Yahr评分为(3.21±0.89)、非快速眼动(NREM)睡眠1期(N1)百分比[(23.56%±13.64)%]、醒觉指数[(54.41±36.45)次/h]、睡眠期周期性腿动指数(5.9次/h)较PD不伴RBD组的相应值[(2.21±0.80)、(11.47%±7.34)%、(26.55±17.25)次/h、1.5次/h]明显升高(P<0.05);而两组患者间的UPDRS -Ⅲ评分、左旋多巴等效剂量、睡眠效率、N2、N3、REM睡眠期百分比及呼吸暂停低通气指数等比较差异无统计学意义.14例PD伴RBD患者中有3例(占21%)出现相关睡眠致伤.结论:同步V-PSG结合临床病史可以提高RBD诊断的准确性.PD伴RBD患者可影响部分睡眠结构,还可能存在相关睡眠致伤的风险.     

肌萎缩侧索硬化症患者睡眠障碍及睡眠呼吸障碍特点分析

目的通过多导睡眠图监测肌萎缩侧索硬化症患者睡眠结构和睡眠呼吸事件,探讨其睡眠障碍和睡眠呼吸障碍特点。方法共36例患者根据是否存在延髓症状分为肢体受累组(14例)和延髓麻痹组(22例),记录一般资料以及睡眠障碍和睡眠呼吸障碍相关主诉,包括入睡困难、睡眠维持困难或早醒、呼吸不畅或鼾症、夜尿症、不宁腿综合征、肌肉疼痛等;Appel肌萎缩侧索硬化症量表(AALS)评价延髓功能、呼吸功能、上下肢肌力和肌肉功能;多导睡眠图监测脑电图、眼动图、心电图、肌电图、体位、鼾声、口鼻气流量、胸腹式呼吸和指端脉搏血氧饱和度,以及睡眠相关参数包括总睡眠时间、睡眠效率、睡眠潜伏期、觉醒次数、非快速眼动睡眠期各期和快速眼动睡眠期比例、睡眠呼吸暂停低通气指数。Pearson相关分析评价快速眼动睡眠期睡眠呼吸暂停低通气指数和周期性腿动与临床资料和AALS评分的相关性。结果延髓麻痹组患者AALS总评分(P=0.007)、延髓功能评分(P=0.000)和呼吸功能评分(P=0.000)高于,上肢肌力(P=0.016)低于肢体受累组。两组患者均出现睡眠结构紊乱,表现为睡眠片段化,其中延髓麻痹组觉醒次数多于(P=0.027)、快速眼动睡眠期比例低于(P=0.009)、周期性腿动次数少于(P=0.020)肢体受累组;两组患者睡眠呼吸障碍主要表现为低通气,其中延髓麻痹组睡眠呼吸暂停低通气指数(P=0.038)、快速眼动睡眠期和非快速眼动睡眠期睡眠呼吸暂停低通气指数(P=0.031,0.049)高于肢体受累组。Pearson相关分析显示,快速眼动睡眠期睡眠呼吸暂停低通气指数与病程(r=0.654,P=0.028)以及AALS总评分(r=0.458,P=0.034)、延髓功能评分(r=0.572,P=0.030)、呼吸功能评分(r=0.756,P=0.002)呈正相关,周期性腿动与病程(r=0.574,P=0.030)以及AALS总评分(r=0.321,P=0.042)、上肢肌肉功能(r=0.656,P=0.028)和下肢肌肉功能(r=0.754,P=0.015)评分呈正相关。结论肌萎缩侧索硬化症患者存在失眠、睡眠呼吸障碍、周期性肢体运动障碍等多种形式的睡眠障碍。多导睡眠图可以监测到睡眠呼吸障碍,为尽早进行无创性正压通气提供临床依据。     

Treatment Considerations in Anticonvulsant Monotherapy

Summary: The long-standing practice of polypharmacy in treating epilepsy is giving way to use of monotherapy. Monotherapy can improve seizure control as well as reduce the risk of serious idiosyncratic reactions, dose-related side effects, and complex drug interactions. Monotherapy also offers improved compliance and cost-effectiveness. The basis of monotherapy is accurate diagnosis and assessment of the patient's seizure type(s), followed by selection of a single appropriate anticonvulsant drug. Many patients currently treated with multiple anticonvulsants can be successfully converted to monotherapy with a carefully monitored program in which troublesome and redundant drugs are gradually withdrawn from the therapeutic regimen.     

Diagnostic Difficulties and Treatment Implications

Summary: Differentiation between types of epileptic seizures has been aided in recent years by the introduction of intensive neurodiagnostic techniques and the development of increasingly detailed classification systems. Paradoxically, these developments have not simplified the task of matching the appropriate antiepileptic drug to a particular seizure type. It is reasonable to assume that anticonvulsant drugs will have different effects on different types of seizures, but faulty, circular reasoning can enter the picture if one also assumes that responses of seizures to different drugs signify different seizure types. There are several examples of differential diagnoses that can fall prey to this problem, including the diagnosis between partial seizures with secondary generalization and generalized tonic-clonic seizures, and the diagnosis between complex partial seizures and absence seizures with automatisms, among others. Considerations of etiology in future classification systems can further complicate the problem: should one then choose an anticonvulsant drug on the basis of individual seizure type or on the basis of the type of epilepsy? Ramifications of this issue extend even to the drug approval process. Official sanction is not given for use of a drug for a seizure type not included in the original efficacy studies, even if later scientific evidence shows that seizure type to be related to a type that is included. New trials must be undertaken. These problems arise from how we choose to classify seizures.     

Cognitive Dysfunction Associated with Antiepileptic Drug Therapy

Summary: Epilepsy is frequently associated with cognitive dysfunction. However, the reasons for this correlation are unclear. Possible influential factors include patient age; duration, frequency, etiology, and type of seizures; hereditary factors; psychosocial issues; and antiepileptic drug (AED) therapy. Whereas many of these factors are beyond the physician's control, AED therapy is one element that can be addressed in treatment decisions by recognizing the potential cognitive effects of particular AEDs. For example, phenobarbital impairs memory and concentration; phenytoin affects attention, problem solving ability, and performance of visuomotor tasks. In contrast, carbamazepine may affect concentration, while valproate would appear to have minimal effects on cognition. Moreover, cognitive effects of AEDs are amplified with coadministration of multiple anticonvulsants (polytherapy). A review of studies on the cognitive effects of monotherapy with AEDs, as opposed to those of polytherapy, provides evidence that drug-related cognitive dysfunction can be reversed if patients are switched to a simpler therapeutic regimen. Future research should be directed toward developing reliable measures for assessing and monitoring cognition, and understanding the particular cognitive side effects of each AED. Physicians also need to revise their opinions about which side effects are "tolerable" for epileptic patients.     

Dextromethorphan: Cellular Effects Reducing Neuronal Hyperactivity

Summary: Dextromethorphan is a dextrorotary morphinan without affinity for opioid receptors, commonly used as an antitussive medication. During the past 5 years, interest in the compound and its demethylated derivative, dextrorphan, has been revived because additional neuroprotective and an-tiepileptic properties were found in in vitro studies, animal experiments, and a few clinical cases. Both morphinans are able to inhibit N -methyl-D-aspartate (NMDA) receptor channels and voltage-operated calcium and sodium channels with different potencies. The inhibition of the NMDA receptor is believed to be the predominant mechanism of action responsible for the anticonvulsant and neuroprotective properties of the compounds.     

Carbamazepine Efficacy in Adults With Partial and Generalized Tonic-Clonic Seizures

Summary: Carbamazepine and phenytoin are drugs of choice in initial monotherapy for adult partial and secondarily generalized tonic-clonic seizures. These designations reflect the results of the Veterans Administration Epilepsy Cooperative Study Group of 1985. An earlier comparative study of carbamazepine and phenytoin by Ramsay and associates found both drugs equally effective in controlling new-onset seizures. Among the advantages of carbamazepine is that it causes relatively few cognitive and dysmorphic side effects. Its disadvantages are its unavailability in parenteral formulation and its metabolic autoinduction. The latter must be compensated for by planned dosage increases to maintain therapeutic plasma steady-state levels during the first 2 or 3 months of treatment. Carbamazepine is judged a drug of choice in the treatment of these secondarily generalized tonic-clonic seizures, and the drug of choice in children, adolescents, and women susceptible to the dysmorphic side effects associated with other anticonvulsant agents.     

Etiologic and Preventive Aspects of Epilepsy in the Child–Bridging the Gap Between Laboratory and Clinic

Summary: Four broad categories of basic phenomena are pertinent to developing ways to prevent epilepsy. These include mechanisms of epileptogenesis, ictal initiation and temporary entrainment by the seizure discharge of normally functioning brain, seizure propagation, and control mechanisms that function both to restrain the cascade of epileptic events culminating in a seizure and to arrest the epileptic event and restore the interictal state. In newborns and children, hypoxia-ischemia is a major factor leading to epileptogenesis, and several schemes are proposed to classify, quantify, and prevent hypoxic-ischemic encephalopathy. Control mechanisms must be better understood in order to develop prophylactic recommendations for epilepsy, and an experimental model of "kindling antagonism" may increase our understanding of these. Programs of prevention of seizures in children will evolve only if basic researchers and clinicians work productively together to develop an adequate understanding of factors important in epileptogenesis and antiepileptogenic control mechanisms.     

Pediatric Epilepsy Surgery

Summary: The use of implantable arrays of epidural electrodes has made it possible to carry out extraoperative electrocorticography (ECoG) and functional localization in the awake child. This has permitted cortical excisions that are determined by criteria similar to those obtained during surgical procedures performed under local anesthesia in adults. In addition, the method also permits simultaneous ECoG and video monitoring during the child's symptomatic seizures, providing additional important localizing information that is impractical to obtain in operations under local anesthesia. We report our experience with 75 children, ages 5 months to 15 years, whom we have managed with epidural electrode arrays. The method of extraoperative ECoG is described and illustrative cases are presented to demonstrate its feasibility and utility in children. In addition, we call attention to gliomas as a common cause of chronic focal seizures in children. Of 49 children undergoing resection and followed for from 1 to 14 years (mean of 5.8 years), 32 (65%) are either seizure free or have had a significant reduction in seizure frequency that has unambiguously improved their quality of life. The results are analyzed further by relating the surgical outcome to each of the pathologic entities that caused the seizures. This analysis reveals the variety of neurological conditions that commonly cause intractable focal seizure disorder in children and distinguishes those pathologic entities in which the seizure disorder is apt to respond to surgical intervention from those that will not.     

Predisposing and Causative Factors in Childhood Epilepsy

Summary: We review information from large studies of defined populations, examining the role of known factors and especially of prenatal and perinatal factors in contributing to nonfebrile seizure disorders of early childhood. We depend especially, but not exclusively, on the recently completed analyses from the Collaborative Perinatal Project of the National Institute of Neurological and Communicative Disorders and Stroke, the NCPP. About 4% of children in the NCPP who had at least one non-febrile nonsymptomatic seizure by the age of 7 years had a previous seizure during acute neurologic illness, such as meningitis or during the acute illness after trauma. Many such seizures should potentially be preventable. Of children with seizures, 10% had had a neonatal seizure and 13% had had a febrile seizure. Among the hundreds of prenatal and perinatal factors explored as predictors of childhood seizure disorders, the principal predictors identified were congenital malformations of the fetus, cerebral and noncerebral; family history of certain neurologic disorders; and neonatal seizures. In agreement with the British National Child Development Study, labor and delivery factors in the NCPP appeared to contribute very little to childhood seizure disorders. Maldevelopment, rather than damage at birth to an initially intact nervous system, appeared to be the more common mechanism. Most seizure disorders of early childhood remained unexplained by the large set of prenatal and perinatal characteristics examined.     

Anticonvulsant Drugs and Cognitive Function: A Review of the Literature

Summary: Alterations of cognitive function are separate from disturbances of behavior seen in association with epilepsy. The nature of the cognitive disability may to a certain extent depend on the seizure type. Partial seizures, mainly derived from a temporal lobe focus, impair memory tasks, while generalized seizures seem to have more effect on attentional abilities. A number of studies, reviewed in this paper, suggest that anticonvulsant drugs further impair cognitive function. Maximal impairments are seen in patients receiving polytherapy: rationalization of polytherapy improves cognitive abilities. Studies in children and adults have allowed differentiation of the effects of various commonly used antiepileptic agents. Maximal cognitive deficits are seen with. phenytoin, while phenobarbital and sodium valproate induce moderate disturbances, and carbamazepine seems relatively free from such toxicity. Further research is needed on the interrelationship between types of seizure disorders, types of anticonvulsant medications, and cognitive function.